Oxidative Stress Induced PC12 Cells Damage: Roles And Mechanisms Of Gap Junctional Communication

Objective:Many evidence indicate that gap junctions between nerve cells involved in pathophysiology of nerve injury. However, the effect of GJ in this process is indirect or direct still ambiguity.Our present studies are aimed at exploring the role of gap junctions in PC12 cells damaged by hydrogen peroxide, and the protective effect of CBX(gap juction inhibitor) and possible mechanisms in that process.Methods:PC12 cells is induced by H2O2 in vitro as oxidative stress, cell viability was tested by MTT assay to establish the optimal concentration and time of H2O2. CBX was used to block the gap junction communication. The open extent of GJ was evaluated by scrape-loading using lucifer-yellow. Morphological changes of apoptosis were shown by AO/EB staining.Result:100μm/L H2O2 caused a significant apoptosis to PC12 cell for 4 hours, simultaneously, extent of GJ communication show expanding. CBX at 100/200μm/L reduced the oxidative damage of PC12 incuced by H2O2(P<0.05). The damage of PC12 cells induced by H2O2 is concerned with the apoptosis signals. Furthermore, blocking the gap junction of PC12 cells inhibit the opoptosis induced by oxidative stress.Conclusions:1. H2O2 induced oxidative damage of PC12 cells concerned with the level of gap junction opening. Gap junction inhibitor can alleviate the extent of damage.2. H2O2 induced oxidative damage of PC12 cells involved in the apoptosis signals,blocking gap junction can alleviate the apoptosis induced by oxidative stress.